# Effect of Fenugreek Extract on Testosterone Propionate-Induced Benign Prostatic Hyperplasia

**Authors:** Jeong Yoon Lee, Jiyoung Bang, Jinhak Kim, Kwang-Soo Baek, Dongchan Oh, Yoo-Hyun Lee

PMC · DOI: 10.3390/ijms26031261 · 2025-01-31

## TL;DR

This study shows that fenugreek extract may help reduce symptoms of benign prostatic hyperplasia in rats by targeting hormone-related and inflammatory pathways.

## Contribution

The study demonstrates fenugreek extract's potential as an alternative treatment for BPH through its effects on androgen and inflammation pathways.

## Key findings

- Fenugreek extract reduced prostate weight and DHT levels in testosterone-induced BPH rats.
- FCT inhibited cell proliferation and decreased expression of androgen and inflammatory markers in BPH-1 cells.
- The extract increased Bax expression and reduced AR, 5α-reductase 2, Bcl-2, IL-6, TNF-α, and NF-κB levels.

## Abstract

Benign prostatic hyperplasia (BPH) is a noncancerous urinary disorder that is common in older adult men; however, its underlying mechanisms remain unclear. Fenugreek has some biological effects, including hyperglycemia regulation, immune response modulation, and anti-cancer properties; In this study, we investigated the ameliorative effects of fenugreek seed extract (Forceterone® [FCT]) in a testosterone propionate (TP)-induced BPH animal model and its mechanisms in BPH-1 human prostate epithelial cells. Sprague Dawley (SD) rats were injected subcutaneously with TP (3 mg/kg) for 8 weeks to induce BPH while FCT was administered orally at 25, 50, and 100 mg/kg. In addition, BPH-1 cells were used to evaluate the inhibitory effects on cell proliferation and examine inflammatory cytokine expression. Treating rats with FCT decreased prostate weight, dihydrotestosterone (DHT) level, and proliferating cell nuclear antigen (PCNA) expression in the prostate. Furthermore, it decreased androgen receptor (AR), 5α-reductase 2, B-cell lymphoma 2 (Bcl-2), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and NF-κB expression in vitro and in vivo and increased Bcl-2-associated X protein (Bax) expression. FCT also inhibited cell proliferation dose dependently in BPH-1 cells. These findings showed the potential use of FCT as an alternative treatment for BPH.

## Linked entities

- **Genes:** AR (androgen receptor) [NCBI Gene 367], BCL2 (BCL2 apoptosis regulator) [NCBI Gene 596], IL6 (interleukin 6) [NCBI Gene 3569], TNF (tumor necrosis factor) [NCBI Gene 7124], NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790], BAX (BCL2 associated X, apoptosis regulator) [NCBI Gene 581], PCNA (proliferating cell nuclear antigen) [NCBI Gene 5111]
- **Chemicals:** testosterone propionate (PubChem CID 5995), dihydrotestosterone (PubChem CID 10635)
- **Diseases:** Benign prostatic hyperplasia (MONDO:0010811), BPH (MONDO:0010811)

## Full-text entities

- **Genes:** AR (androgen receptor) [NCBI Gene 367] {aka AIS, AR8, DHTR, HPCX3, HUMARA, HYSP1}, PCNA (proliferating cell nuclear antigen) [NCBI Gene 5111] {aka ATLD2}, BCL2 (BCL2 apoptosis regulator) [NCBI Gene 596] {aka Bcl-2, PPP1R50}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, BAX (BCL2 associated X, apoptosis regulator) [NCBI Gene 581] {aka BCL2L4}
- **Diseases:** inflammatory (MESH:D007249), BPH (MESH:D011470), urinary disorder (MESH:D014570), hyperglycemia (MESH:D006943), cancer (MESH:D009369)
- **Chemicals:** FCT (-), DHT (MESH:D013196), TP (MESH:D043343)
- **Species:** Trigonella foenum-graecum (fenugreek, species) [taxon 78534], Homo sapiens (human, species) [taxon 9606], Rattus norvegicus (brown rat, species) [taxon 10116]
- **Cell lines:** BPH-1 — Homo sapiens (Human), Benign prostatic hyperplasia, Transformed cell line (CVCL_1091)

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11818512/full.md

---
Source: https://tomesphere.com/paper/PMC11818512